Evidence map›Paper›PMID 42910291›Full record

ArticleInternational journal of biological sciences2026

CYLD: A Key Factor and Novel Predictive Biomarker of Cross-Resistance to Chemotherapy and Radiotherapy in Oral Squamous Cell Carcinoma.

Kou Yonemaru, Naoki Suenaga, Takeshi Masuda, Ryusho Kariya, Yuki Seki, Ryoji Yoshida, Hideki Nakayama, Yoshikazu Kuwahara, Fumihiro Nishimura, Kazutaka Oda and 2 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Kou YonemaruDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Naoki SuenagaDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Takeshi MasudaInstitute for Advanced Biosciences, Keio University, 403-1 Nihonkoku, Daiboji, Tsuruoka-shi, Yamagata 997-0017, Japan.
Ryusho KariyaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811 Japan.
Yuki SekiDepartment of Oral & Maxillofacial Surgery, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ku, Kumamoto, 860-8556 Japan.
Ryoji YoshidaDepartment of Oral & Maxillofacial Surgery, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ku, Kumamoto, 860-8556 Japan.
Hideki NakayamaDepartment of Oral & Maxillofacial Surgery, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ku, Kumamoto, 860-8556 Japan.
Yoshikazu KuwaharaDivision of Radiation Biology and Medicine, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai, Miyagi, Japan.
Fumihiro NishimuraDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Kazutaka OdaDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Jian-Dong LiCenter for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA.
Hirofumi JonoDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cross-resistance to chemotherapy and radiotherapy is a major obstacle in cancer treatment and strongly associated with poor prognosis. Particularly, oral squamous cell carcinoma (OSCC) frequently exhibits such cross-resistance, limiting the efficacy of standard chemoradiotherapy. To unveil its molecular mechanism, we took advantage of a comprehensive proteomic analysis using clinically relevant radio-resistant OSCC cells, and identified distinct alterations in protein expression. Among the differentially expressed proteins, we focused on the down-regulation of cylindromatosis (CYLD), a deubiquitinating enzyme and tumor suppressor. Suppression of CYLD expression in OSCC cells led to accumulation of DNA damage and increased cross-resistance. CYLD down-regulation caused cross-resistance in OSCC cells, at least in part, via NF-κB hyperactivation. Notably, EGFR-TKI monotherapy demonstrated significant efficacy against cross-resistant OSCC

Indexed as

Carcinoma, Squamous CellDeubiquitinating Enzyme CYLDMouth NeoplasmsAnimalsBiomarkers, TumorCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMiceMice, NudeNF-kappa BBiomarkers, TumorCYLD protein, humanDeubiquitinating Enzyme CYLDNF-kappa Bcross-resistancecylindromatosis (CYLD)epidermal growth factor receptor (EGFR)nuclear factor-kappa B (NF-κB)oral squamous cell carcinoma (OSCC)targeted molecular therapy

Identifiers

PMID42910291
PMCPMC13686046

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.